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Correspondence |

Elevation of IL-6 Solely Is Not Sufficient to Infer Systemic Inflammation FREE TO VIEW

Yi-Fong Su, MD; Kun-Ta Chou, MD
Author and Funding Information

From the Chest Department, Taipei Veterans General Hospital.

Correspondence to: Kun-Ta Chou, MD, Chest Department, Taipei Veterans General Hospital, No. 201, Section 2 Shih-Pei Rd, Taipei 112, Taiwan; e-mail: ale1371@yahoo.com.tw


Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;139(1):229-230. doi:10.1378/chest.10-1821
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To the Editor:

In an excellent study in CHEST (July 2010), Sabit et al1 showed that a 2-h hypoxic challenge in patients with mild COPD who are clinically stable results in an elevation of serum IL-6 and some coagulation markers, such as prothrombin activation fragments 1 + 2 and thrombin-antithrombin complex. The authors concluded that a strong association exists between hypoxia, coagulation activation, and systemic inflammation and that patients with COPD may be at increased risk of VTE during air travel.

However, elevation of IL-6 solely cannot be used to infer the presence of systemic inflammation due to the pleiotropic action of IL-6 involving a variety of systems and diseases. IL-6 has been mostly studied in the context of the acute inflammatory response, although growing evidence shows IL-6 also plays a vital role in the pathogenesis of aging and chronic disease.2 In addition, IL-6 is also a “myokine,” a cytokine produced from muscle, and is elevated in response to exercise.3-5 Previous studies have demonstrated IL-6 levels can increase up to 100-fold during exercise, in a duration- and intensity-dependent manner.6,7

In the study by Sabit et al,1 subjects in the group with hypoxia experienced a hypoxic challenge with a mean oxygen saturation decline from 94% ± 2% to 90% ± 3%. When the oxygen concentration in the arterial blood fell, the chemoreceptors were stimulated and the ventilation increased, as shown by a rising respiratory rate (RR) or tidal volume.8 The muscle must be loaded with additional respiratory work, possibly contributing to a surge of IL-6. Although ventilation was not measured, the findings of higher RR and heart rate (HR) in the subjects receiving the hypoxic challenge were also in part compatible with our concern. (In the group with hypoxia, the RR increased from 14 ± 1 per min to 16 ± 3 per min, and the HR increased from 86 ± 6 per min to 94 ± 4 per min; in the control group, the RR increased from 14 ± 1 per min to 15 ± 1 per min, and the HR increased from 82 ± 4 per min to 87 ± 6 per min). In this study, the role of muscle-derived IL-6 should be further clarified in order to accurately document the effect of hypoxia on IL-6.

Sabit R, Thomas P, Shale DJ, Collins P, Linnane SJ. The effects of hypoxia on markers of coagulation and systemic inflammation in patients with COPD. Chest. 2010;1381:47-51. [CrossRef] [PubMed]
 
Maggio M, Guralnik JM, Longo DL, Ferrucci L. Interleukin-6 in aging and chronic disease: a magnificent pathway. J Gerontol A Biol Sci Med Sci. 2006;616:575-584. [CrossRef] [PubMed]
 
Pedersen BK, Febbraio MA. Muscle as an endocrine organ: focus on muscle-derived interleukin-6. Physiol Rev. 2008;884:1379-1406. [CrossRef] [PubMed]
 
Steensberg A, van Hall G, Osada T, Sacchetti M, Saltin B, Klarlund Pedersen B. Production of interleukin-6 in contracting human skeletal muscles can account for the exercise-induced increase in plasma interleukin-6. J Physiol. 2000;529Pt 1:237-242. [CrossRef] [PubMed]
 
Fischer CP. Interleukin-6 in acute exercise and training: what is the biological relevance? Exerc Immunol Rev. 2006;12:6-33. [PubMed]
 
Ostrowski K, Hermann C, Bangash A, Schjerling P, Nielsen JN, Pedersen BK. A trauma-like elevation of plasma cytokines in humans in response to treadmill running. J Physiol. 1998;513Pt 3:889-894. [CrossRef] [PubMed]
 
Pedersen BK, Fischer CP. Physiological roles of muscle-derived interleukin-6 in response to exercise. Curr Opin Clin Nutr Metab Care. 2007;103:265-271. [CrossRef] [PubMed]
 
Guyton AC, Hall JE. Textbook of Medical Physiology. 2006;11th ed Philadelphia, PA Saunders:518-520
 

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References

Sabit R, Thomas P, Shale DJ, Collins P, Linnane SJ. The effects of hypoxia on markers of coagulation and systemic inflammation in patients with COPD. Chest. 2010;1381:47-51. [CrossRef] [PubMed]
 
Maggio M, Guralnik JM, Longo DL, Ferrucci L. Interleukin-6 in aging and chronic disease: a magnificent pathway. J Gerontol A Biol Sci Med Sci. 2006;616:575-584. [CrossRef] [PubMed]
 
Pedersen BK, Febbraio MA. Muscle as an endocrine organ: focus on muscle-derived interleukin-6. Physiol Rev. 2008;884:1379-1406. [CrossRef] [PubMed]
 
Steensberg A, van Hall G, Osada T, Sacchetti M, Saltin B, Klarlund Pedersen B. Production of interleukin-6 in contracting human skeletal muscles can account for the exercise-induced increase in plasma interleukin-6. J Physiol. 2000;529Pt 1:237-242. [CrossRef] [PubMed]
 
Fischer CP. Interleukin-6 in acute exercise and training: what is the biological relevance? Exerc Immunol Rev. 2006;12:6-33. [PubMed]
 
Ostrowski K, Hermann C, Bangash A, Schjerling P, Nielsen JN, Pedersen BK. A trauma-like elevation of plasma cytokines in humans in response to treadmill running. J Physiol. 1998;513Pt 3:889-894. [CrossRef] [PubMed]
 
Pedersen BK, Fischer CP. Physiological roles of muscle-derived interleukin-6 in response to exercise. Curr Opin Clin Nutr Metab Care. 2007;103:265-271. [CrossRef] [PubMed]
 
Guyton AC, Hall JE. Textbook of Medical Physiology. 2006;11th ed Philadelphia, PA Saunders:518-520
 
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